Public Defence: Hélène Spangenberg
MSc Hélène Spangenberg at Institute of Clinical Medicine will be defending the thesis “Cellular mechanisms of vesicle generation and closure” for the degree of PhD (Philosophiae Doctor).
Photo: Trym Erik Nielsen
Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Trial Lecture – time and place
See Trial Lecture.
- First opponent: Assistant Professor Francesca Bottanelli, Freie Universität Berlin, Germany
- Second opponent: Assistant Professor Olof Idevall-Hagren, Uppsala University, Sweden
- Third member and chair of the evaluation committee: Professor II Jørgen Wesche, University of Oslo
Chair of the Defence
Professor II Vessela N. Kristensen, University of Oslo
Assistant Group Leader Camilla Raiborg, University of Oslo
Cells contain membrane-enclosed organelles, also called vesicles, which act as specialized reaction compartments. The formation, the generation of membrane identity, and the closure of vesicles is vital for cells to function properly. Defects in these processes can result in diseases like cancer and neurodegeneration.
In our work, we investigated how vesicles form, generate membrane identity and close. We investigated the first two aspects of vesicle formation and membrane identity generation using the bulk uptake mechanism macropinocytosis as a model pathway. We show that the protein Phafin2 is recruited to forming macropinosomes to guide them through the dense actin cytoskeleton and into the cell. Once formed, nascent macropinosomes need to establish their membrane identity within the cell. We find that both the lipids PtdIns4P and PtdIns3P, as well as RAB proteins play a major role in this process.
In addition, we investigated vesicle closure focusing on a specialized autophagy process, termed mitophagy. Our study shows that recruitment of ESCRT proteins is required to mediate closure of mitophagosomes.
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